Tumor-associated macrophages derived exosomal circPLK1 promotes resistance to EGFR inhibitor osimertinib in non-small cell lung cancer

Abstract Background Circular RNA (circRNA) is involved in the occurrence and development of many cancers. It has been reported that circRNA Polo like kinase 1 (PLK1) is up-regulated in non-small cell lung cancer (NSCLC), but the mechanism of circPLK1 in NSCLC remains to be further explored. Methods...

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Main Authors: Chuankui Li, Xinyu Sun, Zuyi Wang
Format: Article
Language:English
Published: Springer 2025-07-01
Series:Discover Oncology
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Online Access:https://doi.org/10.1007/s12672-025-03025-w
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author Chuankui Li
Xinyu Sun
Zuyi Wang
author_facet Chuankui Li
Xinyu Sun
Zuyi Wang
author_sort Chuankui Li
collection DOAJ
description Abstract Background Circular RNA (circRNA) is involved in the occurrence and development of many cancers. It has been reported that circRNA Polo like kinase 1 (PLK1) is up-regulated in non-small cell lung cancer (NSCLC), but the mechanism of circPLK1 in NSCLC remains to be further explored. Methods THP-1 cells were induced to M2 macrophage polarization to obtain the exosomes from M2 macrophage (M2-Exo). The uptake of M2-Exo and its role in osimertinib (OSI) sensitivity, apoptosis, and activation of Epidermal growth factor receptor (EGFR) were detected. Next, circPLK1 expression and its role on the above mentioned indicators were also detected. The targets of circPLK1 were predicted by CircInteractome. Finally, the regulatory effects of circPLK1 on miRNA and pathways were verified. Results M2 macrophages induced OSI resistance and reduced apoptosis of NSCLC cells. circPLK1 was up-regulated in H1975 cells after co-culture with M2 and M2-Exo. CircPLK1 overexpression decreased OSI sensitivity, inhibited apoptosis, and increased phosphorylation of EGFR in NSCLC cells. miR-186 was a target of circPLK1, and its expression was decreased in M2-Exo and circPLK1 overexpressed NSCLC cells. Further, co-culture with M2-Exo increased the phosphorylation of EGFR, AKT, and extracellular signal-regulated kinase (ERK) in NSCLC cells. miR-186 mimic decreased the levels of phosphorylation of these proteins. In OSI-treated NSCLC cells, circPLK1 overexpression increased the phosphorylation of EGFR, AKT, and ERK in NSCLC cells. miR-186 mimic eliminated the effect of circPLK1 on these proteins in NSCLC cells. Conclusion circPLK1 in exosomes derived from M2-polarized macrophages promotes OSI resistance in NSCLC. Graphical Abstract
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spelling doaj-art-7232d0afff9141249cc3f3d220c238a32025-08-20T03:38:15ZengSpringerDiscover Oncology2730-60112025-07-0116111510.1007/s12672-025-03025-wTumor-associated macrophages derived exosomal circPLK1 promotes resistance to EGFR inhibitor osimertinib in non-small cell lung cancerChuankui Li0Xinyu Sun1Zuyi Wang2Department of Thoracic Surgery, the First Affiliated Hospital of Bengbu Medical UniversityDepartment of Thoracic Surgery, the First Affiliated Hospital of Bengbu Medical UniversityDepartment of Thoracic Surgery, the First Affiliated Hospital of Bengbu Medical UniversityAbstract Background Circular RNA (circRNA) is involved in the occurrence and development of many cancers. It has been reported that circRNA Polo like kinase 1 (PLK1) is up-regulated in non-small cell lung cancer (NSCLC), but the mechanism of circPLK1 in NSCLC remains to be further explored. Methods THP-1 cells were induced to M2 macrophage polarization to obtain the exosomes from M2 macrophage (M2-Exo). The uptake of M2-Exo and its role in osimertinib (OSI) sensitivity, apoptosis, and activation of Epidermal growth factor receptor (EGFR) were detected. Next, circPLK1 expression and its role on the above mentioned indicators were also detected. The targets of circPLK1 were predicted by CircInteractome. Finally, the regulatory effects of circPLK1 on miRNA and pathways were verified. Results M2 macrophages induced OSI resistance and reduced apoptosis of NSCLC cells. circPLK1 was up-regulated in H1975 cells after co-culture with M2 and M2-Exo. CircPLK1 overexpression decreased OSI sensitivity, inhibited apoptosis, and increased phosphorylation of EGFR in NSCLC cells. miR-186 was a target of circPLK1, and its expression was decreased in M2-Exo and circPLK1 overexpressed NSCLC cells. Further, co-culture with M2-Exo increased the phosphorylation of EGFR, AKT, and extracellular signal-regulated kinase (ERK) in NSCLC cells. miR-186 mimic decreased the levels of phosphorylation of these proteins. In OSI-treated NSCLC cells, circPLK1 overexpression increased the phosphorylation of EGFR, AKT, and ERK in NSCLC cells. miR-186 mimic eliminated the effect of circPLK1 on these proteins in NSCLC cells. Conclusion circPLK1 in exosomes derived from M2-polarized macrophages promotes OSI resistance in NSCLC. Graphical Abstracthttps://doi.org/10.1007/s12672-025-03025-wcircPLK1ExosomeEGFROsimertinibNSCLC
spellingShingle Chuankui Li
Xinyu Sun
Zuyi Wang
Tumor-associated macrophages derived exosomal circPLK1 promotes resistance to EGFR inhibitor osimertinib in non-small cell lung cancer
Discover Oncology
circPLK1
Exosome
EGFR
Osimertinib
NSCLC
title Tumor-associated macrophages derived exosomal circPLK1 promotes resistance to EGFR inhibitor osimertinib in non-small cell lung cancer
title_full Tumor-associated macrophages derived exosomal circPLK1 promotes resistance to EGFR inhibitor osimertinib in non-small cell lung cancer
title_fullStr Tumor-associated macrophages derived exosomal circPLK1 promotes resistance to EGFR inhibitor osimertinib in non-small cell lung cancer
title_full_unstemmed Tumor-associated macrophages derived exosomal circPLK1 promotes resistance to EGFR inhibitor osimertinib in non-small cell lung cancer
title_short Tumor-associated macrophages derived exosomal circPLK1 promotes resistance to EGFR inhibitor osimertinib in non-small cell lung cancer
title_sort tumor associated macrophages derived exosomal circplk1 promotes resistance to egfr inhibitor osimertinib in non small cell lung cancer
topic circPLK1
Exosome
EGFR
Osimertinib
NSCLC
url https://doi.org/10.1007/s12672-025-03025-w
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AT xinyusun tumorassociatedmacrophagesderivedexosomalcircplk1promotesresistancetoegfrinhibitorosimertinibinnonsmallcelllungcancer
AT zuyiwang tumorassociatedmacrophagesderivedexosomalcircplk1promotesresistancetoegfrinhibitorosimertinibinnonsmallcelllungcancer